1. Field of the Invention
The present invention relates generally to artificial cardiac pacing, and more particularly to improved pacing electrodes for stimulating or sensing electrical activity of the heart, and to pacing lead assemblies incorporating such electrodes.
2. Prior Art
It is well known that the sinoatrial (S-A) node of the normal mammalian heart acts as the natural pacemaker by which rhythmic electrical excitation is developed and propagated to the atria. In response, the atrial chambers contract, pumping blood into the ventricles. The excitation is propagated the atrioventricular (A-V) node, which imposes a delay, and then via the conduction system consisting of the bundle of His and Purkinge fibers to the ventricular muscle, causing contraction and the pumping of blood from the ventricles. Disruption of this natural pacing/propagation system occurs as a result of aging and disease.
Where normal rate or rhythm is not spontaneously maintained in the heart beat of a human patient, the condition is corrected typically by utilizing an implantable cardiac pacemaker selected according to the particular deficiency of the patient. In its simplest form, the cardiac pacemaker consists of a pulse generator powered by a self-contained battery pack; a lead assembly including an electrode adapted to be positioned in stimulating relationship to excitable myocardial tissue either externally (an epicardial electrode) or internally (an endocardial electrode) of the heart, and an insulated electrically conductive lead interconnecting the pulse generator and the tissue-stimulating electrode to deliver the electrical stimuli to the tissue; and a second electrode connected to a reference potential, by which the electrical circuit is completed via body tissue and fluids. The entire lead assembly is often referred to simply as the lead, and the terminology "lead" and "electrode" are somtimes used interchangeably, albeit inaccurately.
For present purposes, the cardiac tissue-stimulating electrode utilized in the delivery of the pacing stimuli will sometimes be referred to herein as the stimulating cathodic electrode, or simply the cathode, and the other electrode will sometimes be referred to as the anodic electrode, or simply the anode. In fact, however, the coupling may be such that each electrode acts to a certain extent, at different times, as a cathode and an anode. In any event it is well known that activity takes place at each electrode in the delivery of the pacing stimuli.
The customary lead choice for the implantable cardiac pacemaker is an endocardial lead (or leads), because it is readily inserted pervenously to introduce the stimulating electrode into the chamber to be paced. In contrast, an epicardial lead requires thoracic surgery to affix the electrode to the heart. In either case, various means are employed to assure maintenance of positioning of the electrode relative to the excitable heart tissue. For epicardial leads, active fixation such as sutures or a sutureless screw-in electrode is employed. Endocardial leads may utilize active fixation such as a corkscrew, or passive fixation, which is less invasive, in the form of flexible barbs or hooks.
The implanted cardiac pacemaker may utilize a unipolar or bipolar lead system, depending on the preference of the physician and the needs of the patient. With unipolar stimulation, the anode is located remote from the heart, and typically comprises the metal case (or a portion thereof) that houses the batteries, pulse generator and other electronic circuitry of the pacemaker. For bipolar stimulation, the two electrodes are in relatively close proximity to one another, typically with the cathode at the electrode tip for contact with heart tissue, and the anode spaced slightly back from the tip as a ring or sleeve electrode.
In operation, output pulses from the pulse generator are delivered via the lead for electrical stimulation of the excitable myocardial tissue at or in the immediate vicinity of the site of the cathode, to produce the desired rhythmic contractions of the affected chamber. As is well known, stimulation is attributable to current density, and hence small area electrodes will suffice inasmuch as the current required to produce a given current density decreases in direct proportion to the active area of the electrode. Small area electrodes (cathodes) therefore serve to prolong battery life, resulting in a lengthening of the interval between required pacemaker replacements.
In essence, stimulation requires that an electric field of sufficient field strength and current density be impressed on the excitable tissue in the vicinity of the cathode contact site to initiate contraction. The minimum electrical impulse necessary to produce that effect is referred to as the stimulation threshold. The greater the efficiency of the cathode in impressing the electric field on the tissue, the smaller is the amplitude and/or duration of the pulse required to exceed the threshold. Accordingly, highly efficient, low threshold electrodes conserve energy and prolong battery life. Some authorities have theorized that because greater electrode efficiency lowers the energy required for stimulation, it is a factor in reducing injury to tissue at the stimulation site.
The chronic stimulation threshold for a given patient is typically on the order of two to three times greater than the acute threshold observed at the time of implantation and within the first few days thereafter. The increase in threshold is attributed to fibrotic growth; that is, the formation of a layer of non-excitable tissue about the electrode tip at the stimulation site. This fibrotic layer creates a virtual electrode surface area which is considerably greater than the actual surface area of the electrode, and consequently raises the stimulation threshold. Interestingly, the increase of chronic threshold over acute threshold is proportionately greater (to a limit) as electrode area is decreased, presumably because the ratio of virtual to actual surface area is higher for small area electrodes. Many authorities have speculated that the particular composition of the electrode may contribute to or retard fibrotic growth.
Cardiac pacing may be achieved with anodal, rather than cathodal stimulation, but the threshold for the former is higher than that attained with the latter. The reasons for this relate to the polarizing force of the stimulating electric field on ions at the surface of membranes of excitable myocardial cells subjected to the field. Suffice it to note that the highest current density and current flow exist at the side of each affected cell closest to the electrode. A cathodal pulse is depolarizing, or stimulating. In the case of anodal stimulation, however, the effect is hyperpolarizing, or nonstimulating. Reduction of transmembrane potential occurs on the side of each affected cell furthest from the anode, at a point of relatively lower field intensity, which is precisely opposite to the action that occurs with cathodal stimulation. Hence, the threshold for anodal stimulation is higher.
Numerous types of cardiac pacing electrodes have heretofore been developed with these and other factors in mind, utilizing various configurations and materials asserted to promote lower stimulation thresholds and improved electrical efficiencies.